The antifibrotic effects of naringin in a hypochlorous acid (HOCl)-induced mouse model of skin fibrosis. (3rd September 2022)

• Record Type: Journal Article
• Authors: Mohammadi, Mahmoud; Kohan, Leila; Saeidi, Mohsen; Saghaeian Jazi, Marie; Mohammadi, Saeed
• Is Part Of: Immunopharmacology and immunotoxicology. Volume 44:Number 5(2022)
• Page Start: 704
• Page End: 711
• Publication Date: 2022-09-03
• Subjects: Antifibrotic -- fibrosis -- hypochlorous acid (HOCl) -- naringin -- skin; Immunopharmacology -- Periodicals; Immunotoxicology -- Periodicals; Antibody-toxin conjugates -- Periodicals; Immunology -- Periodicals; 615.37
• DOI: 10.1080/08923973.2022.2077217
• Languages: English
• ISSNs: 0892-3973

Abstract

Abstract: Objectives: Fibrosis is a chronic inflammation caused by the loss of innate compensational mechanisms. Naringin (NR) is a flavonoid with antineoplastic and anti-inflammatory effects. Here, we aimed to investigate the antifibrotic effects of NR and underlying mechanisms in a Hypochlorous acid (HOCl)-induced mouse model of skin fibrosis. Materials and methods: A total of 24 six-week-old female BALB/c mice were randomly allocated into five groups: HOCl, Sham, PBS, HOCl + NR and DMSO and selected skin regions were treated for 6 weeks, until sacrifice. The histopathologic and collagenesis of skin resections were analyzed using H&E and PR staining. The mRNA levels of COL1, COL3 and αSMA genes were quantified. Serum samples were also used to evaluate TGF-β levels and LDH activity. Results: HOCl could increase the relative collagen content, while NR administration on HOCl-treated biopsies decreased collagenesis. COL1, COL3 and αSMA mRNA levels were significantly increased among HOCl-treated skin samples, while NR treatment could decrease these mRNA levels of genes to the extent equal to the levels in the Sham group. Similarly, Naringin-treated samples could decrease TGF-β levels. Conclusions: We demonstrated that Naringin could exert protective effects against fibrotic complications of HOCL in skin tissue in vivo, by reducing the collagenesis and decreasing the levels of fibrosis-associated genes.